Cadmium-induced testicular damage is associated with mineral imbalance, increased antioxidant enzymes activity and protein oxidation in rats

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Currently, the spectrum of pathological manifestations associated with cadmium-induced testicular toxicity is poorly understood. Thus, we investigated the impact of cadmium (Cd) exposure on testicular mineral bioavailability, activity of antioxidant enzymes, testicular structure and germ cells ultrastructure

Main methods:

Cadmium chloride was administered in a single dose to thirty rats equally randomized into five groups: Saline, 0.9% NaCl; Cd1 – Cd4, 0.67, 0.74, 0.86 and 1.1 mg Cd/kg. Seven days after Cd exposure, animals were euthanized and testes were collected for biochemical analysis, as well as light, scanning and transmission electron microscopy.

Key findings:

Cadmium exposure induced dose-dependent testicular toxicity. Tubular and intertubular compartments were targets of Cd and calcium (Ca) deposits, marked structural and ultrastructural pathologic remodeling, and a reduced distribution of iron, selenium, magnesium, copper, zinc and total protein. Despite upregulation in antioxidant enzyme activities (i.e. catalase [CAT] and superoxide dismutase [SOD]), morphologic and molecular testis damage such as protein oxidation was not prevented, especially with higher doses of Cd. As non-degenerated tissue areas also presented Ca deposits, Ca imbalance was not only a consequence but also a cause of Cd-induced testis toxicity and germ cell death


Taken together, our findings indicated that Cd exposition induced dose-dependent testicular dystrophic calcification, which was associated with increased antioxidant enzymes activity and protein oxidation, mineral imbalance, germ cell calcification and death in rats. Although increased CAT and SOD activity represents a counter-regulatory reaction to cadmium-induced toxicity, this reaction is insufficient to prevent testicular pathological remodeling.

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